Inhaled nanoparticles – like those released from vehicle exhausts – can work their way through the lungs and into the bloodstream, potentially raising the risk of heart attack and stroke, according to new research part-funded by the British Heart Foundation. The findings, published today in the journal ACS Nano, build on previous studies that have found tiny particles in air pollution are associated with an increased risk of cardiovascular disease, although the cause remains unproven. However, this research shows for the first time that inhaled nanoparticles can gain access to the blood in healthy individuals and people at risk of stroke. Most worryingly, these nanoparticles tend to build-up in diseased blood vessels where they could worsen coronary heart disease – the cause of a heart attack.

It is not currently possible to measure environmental nanoparticles in the blood. So, researchers from the University of Edinburgh, and the National Institute for Public Healthand the Environment in the Netherlands, used a variety of specialist techniques to track the fate of harmless gold nanoparticles breathed in by volunteers. They were able to show that these nanoparticles can migrate from the lungs and into the bloodstream within 24 hours after exposure and were still detectable in the bloodthree months later. By looking at surgically removed plaques from people at high risk of stroke they were also able to find that the nanoparticles accumulated in the fatty plaques that grow inside blood vessels and cause heart attacks and strokes. Cardiovascular disease (CVD) – the main forms of which are coronary heart disease and stroke – accounts for 80% of all premature deaths from air pollution.

“It is striking that particles in the air we breathe can get into our blood where they can be carried to different organs of the body. Only a very small proportion of inhaled particles will do this, however, if reactive particles like those in air pollution then reach susceptible areas of the body then even this small number of particles might have serious consequences,” said Dr Mark Miller, Senior Research Fellow at the University of Edinburgh who led the study.

As men and women grow older, their chances for coronary heart disease also increase. Atherosclerosis is a condition in which plaque builds up inside the arteries, which can lead to serious problems, including heart attacks, strokes or even death. Now, researchers at the University of Missouri (MU) have found that Insulin-like Growth Factor-1 (IGF-1), a protein that is naturally found in high levels among adolescents, can help prevent arteries from clogging. They say that increasing atherosclerosis patients’ levels of the protein could reduce the amount of plaque buildup in their arteries, lowering their risk of heart disease.

“The body already works to remove plaque from arteries through certain types of white blood cells called macrophages,” said Yusuke Higashi, PhD, assistant research professor in the Division of Cardiovascular Medicine at the MU School of Medicine and lead author of the study. “However, as we age, macrophages are not able to remove plaque from the arteries as easily. Our findings suggest that increasing IGF-1 in macrophages could be the basis for new approaches to reduce clogged arteries and promote plaque stability in aging populations.”

In a previous study, Higashi and Patrice Delafontaine, MD, the Hugh E. and Sarah D. Stephenson Dean of the MU School of Medicine, examined the arteries of mice fed a high-fat diet for eight weeks. IGF-1 was administered to one group of mice. Researchers found that the arteries of mice with higher levels of IGF-1 had significantly less plaque than mice that did not receive the protein. Since the macrophage is a key player in the development of atherosclerosis, the researchers decided to investigate potential anti-atherosclerosis effects of IGF-1 in macrophages. The team also found that the lack of IGF-1 action in macrophages changed the composition of the plaque, weakening its strength and making it more likely to rupture and cause a heart attack.